ABSTRACT
Objective To observe the toxicity of diesel exhaust particles extracts(DEPE) on V79 cell in cell viability, membrane and oxidative stress. Methods Cell exposed different concentrations of DEPE for different time , the change of cell viability, the leakage of intracellular lactate dehydrogenase(LDH), intracellular glutathione(GSH) and glutathione peroxidase (GPX)content were determined respectively, and analyzed the relation between GSH and GPX. Results The results showed that the viability of V79 cell decreased and the leakage rate of lactate dehydrogenase increased gradually in according with the increasing dosage of DEPE,and that DEPE could impair V79 cell by oxidative stress, included intracellular GSH content decreased and the activity of GPX increased, indicating that GPX might play a important role in DEPE induced GSH depletion. Conclusion DEPE may impair cell viability and the cell membrane integrity, also impair cell by oxidative stress.
ABSTRACT
Objective To explore the effects of prenatal exposure to lead on learning and memory of rats' offspring. Methods The pregnant rats were randomly divided into 4 groups provided with double evaporated water, 50, 100 and 200 mg/L lead acetate solution via drinking water respectively. The lead-exposure period for exposure groups was limited from the 1st day after pregnancy to the 20th day when the offspring began to be weaned. For learning ability 20-day old offspring were tested by water maze. For active learning and memory ability, the 20-day old, 40-day old and 60-day old offspring were tested by Y maze. Results The frequency of the mistakes in water maze made by offspring increased with the increase of the prenatal lead-exposure doses of their mothers and showed significantly higher levels in 100 and 200 mg/L groups compared with that of control group (P0.05). But the qualified rates of 0-min and 24-h escape for 100 and 200 mg/L groups showed sigificantly lower levels compared with that of control group when they were 60-day old (P
ABSTRACT
The progress of mainly experimental studies on the chronic toxicity test of the automobile exhaust-involving reproductive system impairment, chronic lung impairment and lung cancer in this paper, and the general situation and the progress on the latest domestic and foreign studies on the possiblely multiple mechanisms of automobile exhaust-induced chronic toxicity are introduced. Some epidemiological study results on the automobile exhausts-induced chronic impairments are reviewed, as well as some problems required to be explored further in the occupational risk assessment of exposure to automobile exhausts in recent years.
ABSTRACT
Objective To study the effects of zinc-metallothionein (ZnMT) on the cadmium-induced oxidative damage of liver and kidney in mice. Methods The model of laboratory animal was established by 14 d-cadmium exposure to Kunming mice. Then the cadmium-poisoning mice were grouped as Cd-ZnMT group and Cd-ZnSO4 group and perfused orally by solution of ZnMT and ZnSO4 for 14 days respectively. The morphological changes of liver and kidney were observed by electron microscope. The contents of malonydiadehyde (MDA), the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in supernatant fluid of liver and kidney were determined. Results The decreases of the contents of MDA, the increases of the activities of SOD and GSH-Px in liver and kidney of mice in Cd-ZnMT and Cd-ZnSO4-exposure group were observed compared with those in cadmium-exposure group, the dose-effect relationships were also found. The increases of the activities of SOD and GSH-Px, the decrease of contents of MDA of liver and kidney, were found in Cd-ZnMT-exposure group compared with those of Cd-ZnSO4-exposure group, but without statistical significances. The morphological damages of liver and kidney observed by electron microscope in mice of cadmium-exposure group were more serious than those in mice treated with solution of ZnMT and ZnSO4 after cadmium exposure. Conclusion ZnMT could repair the lipid peroxidative damages in liver and kidney in mice induced by exposure to cadmium in a certain degree.